Why was the E coli outbreak so deadly?

Researchers in Germany have been investigating why the recent E coli outbreak in Europe had a high mortality rate.

They believe they have narrowed down the reason for the deadly character of the outbreak to a rare strain of the bacterium, 0104:H4.

The strain combines elements of two different pathogens: the ability of the enterohaemorrhagic E coli (EHEC) to produce shiga toxin, and the ability of enteroaggregative E coli (EAEC) to stick in the gut.

The European outbreak, the deadliest known to be caused by E coli in history, is a clone that combines the two qualities, according to a report published in The Lancet Infectious Diseases.

This, the researchers say, might explain its greater virulence and the unusually high number of infections resulting in complications and death.

Straightforward infection with EHEC usually leads to complete recovery with treatment, with only 10% of patients experiencing serious complications, which can include haemolytic uraemic syndrome (HUS), a potentially fatal form of kidney failure.

Up until June 20, Germany had reported a total of 810 HUS cases this year, compared with an average number of just 60 in any other whole year.

In the same period, German doctors saw 2,684 cases of E. coli which produced shiga toxin, compared with 1,000 in an average year.

Lead author Helge Karch from the University of Munster began the study to gain a better understanding of the greater virulence of this year's outbreak of E coli.

Karch and her team analysed 80 bacteria samples from patients in this year's outbreak, testing them both for shiga toxin and other virulence genes found in different strains of E coli.

The samples were also examined for their susceptibility to antibiotics, their ability to stick to cells in the gut lining, and other underlying characteristics.

They found that all of the samples produced both the shiga toxin and the ability to stick in the gut.

They also found that the strain in this year's outbreak showed signs of resistance to all penicillin and cephalosporin antibiotics. However, they remained susceptible to carbapenems.

They said that the combination of features was a deadly one, because the greater sticking power might aid greater absorption of shiga toxin in the gut of those infected.

This could explain the high frequency of progression to HUS, they speculated.

The outbreak showed how blended virulence characteristics could have serious consequences for patients, with tragic results, they concluded.

However, they said they lacked an explanation for the increased virulence.